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Infection and Immunity, May 2009, p. 1881-1887, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.00030-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Langerhans Cell Deficiency Impairs Ixodes scapularis Suppression of Th1 Responses in Mice{triangledown}

Diana L. Vesely,1 Durland Fish,2 Mark J. Shlomchik,3 Daniel H. Kaplan,4 and Linda K. Bockenstedt1*

Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520,1 Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut 06520,2 Departments of Laboratory Medicine and Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520,3 Department of Dermatology, Center for Immunology, University of Minnesota, Minneapolis, Minnesota 554554

Received 8 January 2009/ Returned for modification 9 February 2009/ Accepted 28 February 2009

Ixodes scapularis ticks transmit a number of human pathogens, including the Lyme disease spirochete Borrelia burgdorferi. I. scapularis suppresses host immunity in the skin to promote feeding and systemically skew T-helper (Th)-cell differentiation toward Th2 cells in secondary lymphoid organs. Although components of tick saliva are known to influence Th-cell polarization, the mechanism whereby tick feeding in the skin modulates regional and systemic Th-cell responses is unknown. In this study, the role of the epidermal Langerhans cell (LC) subset of skin dendritic cells in tick-mediated Th1/Th2-cell immunomodulation was assessed. Mice deficient in LCs (Langerin-DTA mice) exhibited enhanced lymph node (LN) concanavalin A (ConA)-induced Th1 responses after tick infestation in comparison to results for uninfested Langerin-DTA or wild-type (WT) mice, whereas effects on Th2-cell production of interleukin 4 were more variable. Nonetheless, the altered T-cell response did not impact tick feeding or refeeding. Gamma interferon production by ConA-stimulated LN cells of both WT and LC-deficient mice was enhanced by as much as fourfold after B. burgdorferi-infected-tick feeding, indicating that immunomodulatory effects of tick saliva were not able to attenuate the Th1 immune responses induced by this pathogen. Taken together, these findings show a requirement for LCs in the tick-mediated attenuation of Th1 responses in regional lymph nodes but not in the spleens of mice and show that the presence of a pathogen can overcome the Th1-inhibitory effects of tick feeding on the host.

* Corresponding author. Mailing address: Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, TAC S-520, 300 Cedar Street, New Haven, CT 06520. Phone: (203) 785-2453. Fax: (203) 785-7053. E-mail: Linda.Bockenstedt{at}yale.edu

{triangledown} Published ahead of print on 9 March 2009.

Editor: S. R. Blanke

Infection and Immunity, May 2009, p. 1881-1887, Vol. 77, No. 5
0019-9567/09/$08.00+0     doi:10.1128/IAI.00030-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

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